Linear acceleration-evoked cardiovascular responses in awake rats

Abstract

It has been well documented that vestibular-mediated cardiovascular regulation plays an important role in maintaining stable blood pressure (BP) during postural changes. But the underlying neural mechanisms remain to be elucidated. In particular, because the vestibular stimulation employed in previous animal studies activated both semicircular canals and otolith organs, the contributions of the otolith system has not been studied selectively. The goal of the present study was to characterize cardiovascular responses to natural otolith stimulation in awake rats that were subjected to pure linear motion. In any of the four directions tested, transient linear motion produced a short-latency ( approximately 520 ms) increase in mean BP with a peak of 8.27 +/- 0.66 mmHg and was followed by a decrease in BP. There was an initial small biphasic response in heart rate (HR) that was followed by a longer duration increase. The short-latency increase in BP was absent in rats that were pentobarbital sodium anesthetized or that were labyrinthectomized bilaterally, but it was unaffected by baroreceptor denervation, indicating that it was of otolith origin. The increase in BP was linear acceleration intensity dependent and was not affected by absence of visual cues. Furthermore, the BP response was attenuated by inactivation of the medial and inferior vestibular nuclei by microinjections of muscimol, indicating that the otolith-driven cardiovascular responses are mediated by the neurons in these areas. These results not only demonstrate the otolith specific influences on the cardiovascular system but also they establish the first rodent model for examining the neural mechanisms underlying the otolith-mediated cardiovascular regulation.

What Does Galvanic Vestibular Stimulation Actually Activate?

“…When sGVS is applied to anesthetized rats, it can also induce sudden decreases in blood pressure and heart rate that resemble human vasovagal syncope (Cohen et al, 2011). Similar sustained drops in blood pressure have been shown in alert and anesthetized rats after linear acceleration (Zhu et al, 2007). sGVS also evokes frequency-dependent postural sway in standing subjects, further supporting the idea that the stimulus primarily activates the otolith system (Lau et al, 2003).…”

Sinusoidal galvanic vestibular stimulation (sGVS) induces a vasovagal response in the rat

“…Tilts in the roll plane were ineffective in our study, consistent with findings in normal cats, in which only nose-up but not roll stimulation produce cardiovascular responses (Yates and Miller 1994; Yates 1996; Woodring et al 1997). However, linear oscillation about any axis in the horizontal plane produces similar 7–9 mmHg oscillations of BP (Yates et al 1999; Zhu et al 2007). Many studies indicate that BP and HR responses to sinusoidal oscillation in pitch are of otolith origin (Lindsay et al 1945; Spiegel 1946; Megirian and Manning 1967; Tang and Gernandt 1969; Uchino et al 1970; Doba and Reis 1974; Ishikawa et al 1979; Ishikawa and Miyazawa 1980; Yates et al 1993b; Kerman and Yates 1998; Jian et al 1999; Kerman et al 2000).…”

Intravestibular Balance and Motion Sickness

“…24 Regardless of the exact scenario, the fact that sympathomimetics like dextroamphetamine reduce MS symptoms while parasympathetic blockers such as cholinergic (muscarinic) antagonists attenuate MS-induced vomiting clearly supports the role of parasympathetic dominance in MS. 103 The role of the vestibular system in autonomic control is also complex and remains controversial in some areas. On the basis of a wide range of evidence, including effects on blood pressure 51,111 and sympathetic muscle activity, 14,44,51 Yates et al 105 concluded that the otoliths have a primarily sympathetic influence on cardiovascular output, which makes sense in that changes in head position relative to gravity are sensed primarily by the otolith organs and they, in turn, send a signal to boost cardiac output before blood pressure drops are detected by the baroreceptors. 105 The canals do not appear to mediate the vestibulo-sympathetic response 82 and, if anything, may exert more of a parasympathetic influence.…”